A team of researchers has developed specialized antibody-like receptor proteins that they believe could soak up the excess cytokines produced during a cytokine storm. This excessive immune response, sometimes seen in Covid-19 patients, can be fatal. Treating the potential cytokine storm, seen in Virus patients could be the alternative to vaccines. Cytokine Storms, an autoimmune response. Instead of vaccine,

Cytokine storm in the lung following severe influenza infection. (1) Viruses infect lung epithelial cells and alveolar macrophages to produce progeny viruses and release cytokines/chemokines (mainly contains interferons). (2) Cytokine/chemokine-activated macrophages and virally infected dendritic cells lead to a more extensive immune response and the initiation of cytokine storm. (3) Released chemokines attract more inflammatory cells to migrate from blood vessels into the site of inflammation, and these cells release additional chemokines/cytokines to amplify cytokine storm.

https://www.nature.com/articles/cmi201574

So A cytokine storm is an overproduction of immune cells and their activating compounds (cytokines), which, in a flu infection, is often associated with a surge of activated immune cells into the lungs. The resulting lung inflammation and fluid buildup can lead to respiratory distress and can be contaminated by a secondary bacterial pneumonia -- often enhancing the mortality in patients.

Proteins may halt the severe cytokine storms seen in COVID-19 patients

Team designs antibody-like receptor proteins that can bind to cytokines, as possible strategy for treating coronavirus and other infections

Date:

April 16, 2020

Source:

Massachusetts Institute of Technology

Summary:

A team of researchers has developed specialized antibody-like receptor proteins that they believe could soak up the excess cytokines produced during a cytokine storm. This excessive immune response, sometimes seen in Covid-19 patients, can be fatal.

https://www.sciencedaily.com/releases/2020/04/200416135950.htm

cytokine

/ˈsʌɪtə(ʊ)kʌɪn/

Learn to pronounce

noun

PHYSIOLOGY

1. any of a number of substances, such as interferon, interleukin, and growth factors, which are secreted by certain cells of the immune system and have an effect on other cells.

A few months back I watched David Icke explain in a program that what actually is killing people isn't the virus but, in the elderly and those with different health conditions, (and those with certain dna markers) it was a 'Stressed' auto immune reaction to the virus which presents as a sudden and violent release of cytokines. This 'storm of cytokines'  White blood cells and fighter cells set to kill invading cells, will flood in a aggressive response to the detection of a viral entity in the body. Cytokines do this. That's what they do, it is Usually a normal healthy response. But to bodies that have endured years of stress and or over medication, (think: elderly person, living through years of enduring situations etc, 19 medications per day) and the same for people whose health has been compromised by stress or an overexposure to chemicals etc etc. the immune response will be a flair up of cytokines, as in a storm, and it is this which has the capacity to kill. It is the pathway that an already compromised immune system will inevitably go down, and is significantly higher for certain types of people that have certain biological markers that will be predisposed to a cytokine storm 'emergency room' situation...when they have come across infection with a virulent virus. AND...and it is true too, when a small amount of  'dead' Virulent virus (with other foreign ingredients, in a vaccine) is injected into these already stress/health compromised people or those with culturally identified biological markers that will trigger such a cytokine storm release, which can and do kill..... 
In both a 'natural' situation of an organic, randomly 'occurring in nature',  'biologically aggressive' and in an unnatural situation whereby a virus has been manipulated to swarm and mutate in an aggressive manner, then it is especially difficult to determine a death directly from the virus...or death by this cytokine storm, as it floods to lungs, triggered by the virus.

It seems that some types of 'genes on the protein of a flu virus (a marker) actively can, and do strongly activate this cytokine storm response in certain types of individuals: So certain genes are known to activate cytokine storms when certain types of people are infected wuth certain types of flu virus. i.e  they are a Known component of a flu virus.
evidence in mice that infection with influenza virus carrying the HA gene from the 1918 virus seems to strongly activate some immune cells to over-produce a half dozen or more cytokines

Weathering the cytokine storm in COVID-19: Telltale signs, therapeutic hope on the horizon

April 14, 2020

Randy Q. Cron

Good news about COVID-19 is at a premium these days. Encouraging reports about therapeutic options or vaccine development usually are either overly optimistic or entirely spurious. But scientific advancement is as relentless as the virus itself, and this is exemplified by a growing body of research into a potential association between cytokine storm syndrome and COVID-19.

Randy Q. Cron, MD, PhD, of the Children’s Hospital of Alabama and the University of Alabama at Birmingham, described cytokine storm syndrome as an “overly exuberant” immune response to something like a viral infection or cancer. While it is not currently known why some patients with COVID-19 demonstrate this response and others do not, plenty is known about these inflammatory immunologic proteins and how they have reacted in other disease states, many of them rheumatologic conditions.

Deadly immune 'storm' caused by emergent flu infections

Date:

February 27, 2014

Source:

The Scripps Research Institute

Summary:

Scientists have mapped key elements of a severe immune overreaction -— a “cytokine storm” -— that can both sicken and kill patients who are infected with certain strains of flu virus. A cytokine storm is an overproduction of immune cells and their activating compounds (cytokines), which, in a flu infection, is often associated with a surge of activated immune cells into the lungs. The resulting lung inflammation and fluid buildup can lead to respiratory distress and can be contaminated by a secondary bacterial pneumonia -- often enhancing the mortality in patients.

Scientists at The Scripps Research Institute (TSRI) have mapped key elements of a severe immune overreaction -- a "cytokine storm" -- that can both sicken and kill patients who are infected with certain strains of flu virus.

Their findings, published in this week's online Early Edition of the Proceedings of the National Academy of Sciences, also clarify the workings of a potent new class of anti-inflammatory compounds that prevent this immune overreaction in animal models.

"We show that with this type of drug, we can quiet the storm enough to interfere with the virus-induced disease and lung injury, while still allowing the infected host to mount a sufficient immune response to eliminate the virus," said John R. Teijaro, an assistant professor in TSRI's Department of Immunology and Microbial Science and first author of the study.

"This study provides insights into mechanisms that are chemically tractable and can modulate these cytokine storms," said Hugh Rosen, professor in TSRI's Department of Chemical Physiology and senior author of the study with Michael B. A. Oldstone, professor in TSRI's Department of Immunology and Microbial Science.

Calming the Storm

A cytokine storm is an overproduction of immune cells and their activating compounds (cytokines), which, in a flu infection, is often associated with a surge of activated immune cells into the lungs. The resulting lung inflammation and fluid buildup can lead to respiratory distress and can be contaminated by a secondary bacterial pneumonia -- often enhancing the mortality in patients.

This little-understood phenomenon is thought to occur in at least several types of infections and autoimmune conditions, but it appears to be particularly relevant in outbreaks of new flu variants. Cytokine storm is now seen as a likely major cause of mortality in the 1918-20 "Spanish flu" -- which killed more than 50 million people worldwide -- and the H1N1 "swine flu" and H5N1 "bird flu" of recent years. In these epidemics, the patients most likely to die were relatively young adults with apparently strong immune reactions to the infection -- whereas ordinary seasonal flu epidemics disproportionately affect the very young and the elderly.

For the past eight years, Rosen's and Oldstone's laboratories have collaborated in analyzing the cytokine storm and finding treatments for it. In 2011, led by Teijaro, who was then a research associate in the Oldstone Lab, the TSRI team identified endothelial cells lining blood vessels in the lungs as the central orchestrators of the cytokine storm and immune cell infiltration during H1N1 flu infection.

In a separate study, the TSRI researchers found that they could quiet this harmful reaction in flu-infected mice and ferrets by using a candidate drug compound to activate immune-damping receptors (S1P1 receptors) on the same endothelial cells. This prevented most of the usual mortality from H1N1 infection -- and did so much more effectively than the existing antiviral drug oseltamivir, although the combination of both therapies worked even better. "That was really the first demonstration that inhibiting the cytokine storm is protective," said Teijaro.

Cytokine Storm

https://www.sinobiological.com/resource/cytokines/cytokine-storm

What is Cytokine Storm

The cytokine storm has captured the attention of the public and the scientific community alike, and while the general notion of an excessive or uncontrolled release of proinflammatory cytokines is well known, the concept of a cytokine storm and the biological consequences of cytokine overproduction are not clearly defined. Cytokine storms are associated with a wide variety of infectious and noninfectious diseases. The term was popularized largely in the context of avian H5N1 influenza virus infection, bringing the term into popular media.

In 1993 a group in Boston, perhaps mindful of the recent Desert Storm war, coined "cytokine storm" to describe their observations in graft-versus-host disease (GVHD). The term next appeared in 2002 as a description of the disease mechanism in pancreatitis. As with GVHD, the idea was older than the aptly descriptive term, with a pro- and an anti-inflammatory cytokine being incriminated in this condition in 1992 and 1997, respectively. The first use of cytokine storm to describe the mechanism of an infectious disease was probably observed a year later, in 2003, in influenza encephalopathy. Subsequently, it was applied to variola virus and H5N1 influenza.

Cytokine storm symptoms

Cytokine storm syndromes (CSS) are a group of disorders representing a variety of inflammatory causes. The primary symptoms of a cytokine storm are high fever, swelling and redness, extreme fatigue and nausea. In some cases the immune reaction may be fatal.

Cytokine storm causes

When the immune system is fighting pathogens, cytokines signal immune cells such as T-cells and macrophages to travel to the site of infection. In addition, cytokines activate those cells, stimulating them to produce more cytokines. Normally, this feedback loop is kept in check by the body. However, in some instances, the reaction becomes uncontrolled, and too many immune cells are activated in a single place. The precise reason for this is not entirely understood but may be caused by an exaggerated response when the immune system encounters a new and highly pathogenic invader. Cytokine storms have potential to do significant damage to body tissues and organs. If a cytokine storm occurs in the lungs, for example, fluids and immune cells such as macrophages may accumulate and eventually block off the airways, potentially resulting in death.

The cytokine storm (hypercytokinemia) is the systemic expression of a healthy and vigorous immune system resulting in the release of more than 150 known inflammatory mediators (cytokines, oxygen free radicals, and coagulation factors). Both pro-inflammatory cytokines (such as Tumor necrosis factor-alpha, Interleukin-1, and Interleukin-6) and anti-inflammatory cytokines (such as interleukin 10 and interleukin 1 receptor antagonist) are elevated in the serum of patients experiencing a cytokine storm.

Cytokine Storm Treatment

The clinical presentations of all cytokine storm symptoms (CSS) can be strikingly similar, creating diagnostic uncertainty. However, clinicians should avoid the temptation to treat all CSS equally, because their inciting inflammatory insults vary widely. Failure to identify and address this underlying trigger results in delayed, inoptimal, or potentially harmful consequences.

Drugs for the treatment of cytokine storm can be classified into the following types: OX40 IG, ACE inhibitors and Angiotensin II Receptor Blockers, Corticosteroids, Gemfibrozil, Free radical scavengers, TNF-alpha blockers.

Cytokine Storm Influenza

The occurrence of a “cytokine storm” has been suggested as an explanation for the devastating nature of the 1918 influenza pandemic and perhaps H5N1 influenza. Influenza is thought to be one of the rare conditions able to cause a cytokine storm. Cytokine dysregulation is involved in other syndromes with symptoms much like those seen in complicated influenza (e.g., toxic shock syndrome or gram negative sepsis). In these cases the causes are more related to “always on” T-cell activation (stuck accelerator). Whether “always on” activation and thus continuous pro-inflammatory cytokine production, some other kind of cytokine dysregulation, or nothing to do with cytokines happens in influenza is still open to question. The strongest evidence comes from the clinical presentation of virulent influenza cases and the evidence in mice that infection with influenza virus carrying the HA gene from the 1918 virus seems to strongly activate some immune cells to over-produce a half dozen or more cytokines.